Efeito do ganho de peso sobre o metabolismo ósseo maxilar de ratos

Abstract

Periodontitis main etiological factor is the exacerbated immune response of the host to specific microorganisms and may have its severity increased when associated with systemic disorders such as diabetes and obesity. Obesity is a chronic disorder capable of inducing injury to the health of an individual as well as the onset of other chronic illnesses. Exacerbation of the release of proinflammatory cytokines into the bloodstream appears to be the main factor that justifies the increased severity of periodontal disease in obese individuals. Regarding bone tissue, obesity seems to be associated with low mineral density by stimulating osteoclast activity, by the presence of proinflammatory cytokines such as interleukin (IL)-1ß, IL-6, tumor necrosis factor alpha (TNF-a), which modulates the axis of the receptor activator of nuclear factor-kappa B (RANK), its ligand (RANKL) and the false decoy osteoprotegerin (OPG). The objective of this study was to evaluate by morphometry the effect of the weight gain on the periodontal bone tissue of rats. Animals were divided equally in two groups one fed with balanced ration (control) and another with hyperlipidic diet cafeteria-type (obese). In the first manuscript, we analyzed the alveolar bone of the mandibles of the rats using computerized microtomography in order to relate the weight gain with possible changes in the microstructure of the alveolar bone. In the rats that became obese, the alveolar bone in the interradicular septum was gradually reduced and the trabecular bone partially replaced by a more cancellous bone, there was also a decrease in the contact between the alveolar bone and the tooth, reinforcing the bone loss in this region. In the second manuscript, after 6 weeks of standard diet and hyperlipidic diet, the animals underwent surgery to remove the upper right incisor, receiving postoperative care. In the post-exodontia periods (7, 14 and 28 days) the animals were sacrificed and the right maxilla preserved in 10% formalin for later histological processing. The histological sections were stained with hematoxylin-eosin for histomorphometric evaluation and the immunohistochemical reaction was performed to evaluate the expression of OPG, RANKL, osteocalcin and tartrate resistant acid phosphatase (TRAP). In the histomorphometric evaluation, the obese group presented later repair when compared to the control group. There was an increase in the expression of TRAP at the extraction site, probably induced by the elevation of the RANKL labelling, which would justify the delay of the alveolar bone repair in the areas of dental extraction. In general, our studies suggest that obesity interferes with alveolar bone metabolism leading to reduction of trabecular bone and in the bone area, as well as a delay the repair of dental alveoli.